Hello, great video! One question: the "Synthesis & reuptake" part - can you tell me the exact sources that you used for that part. I'm well aware you've got all your sources in the description, but I'd like to read the exact source. Thank you
@sciencewithtal
7 ай бұрын
Hi, I used the textbook Principles of Neural Science (6th version) to cover this section. The passage that discusses this topic of the video is in chapter 16 (neurotransmitters) and there is a figure (Fig 16-1) that illustrates the reuptake process. If you do not have the textbook, send me an email at sciencewithtal@gmail.com and I'll send you the figure. Hope this helps!
@violettebri
7 ай бұрын
Thank you so much! I appreciate you replying to quick as you did. I'm currently writing an exam and this was so helpful. @@sciencewithtal
@sciencewithtal
7 ай бұрын
@@violettebri My pleasure, good luck!
@violettebri
3 ай бұрын
@@sciencewithtal I finished my exam with an A !!, and I wanted to say thank you so much! I've been watching your videos throughout this exam period, and they truly helped me gain a visual understanding of the material. Have a great summer!
@sciencewithtal
3 ай бұрын
@@violettebri Glad I could help, good job!!!
@lukasin6242
8 ай бұрын
When GABA is released, it connects to both GABA A and GABA B recpetors?
@sciencewithtal
8 ай бұрын
Yes, GABA is an agonist/ligand for both receptors. It will bind to both if GABA A and GABA B receptors are both present on the postsynaptic neuron. Let me know if there is anything else!
@christinefarneman4433
2 ай бұрын
Thank you! But I am a little confused about glycine. The thing is that I feel awful when I take magnesiumglycinatet which contain around 2 grams of glycine. I read that glycine can active NMDA and glutamate. I watched your other video about NMDA and felt that that's why I didn't feel good when I take glycine. But in this video you said glycine is an inhibitory transmittor. Can you our someone explain to me how I make glycine inhibitory? Thanks!
@sciencewithtal
2 ай бұрын
Hi, sorry to hear that it makes you feel awful. I think you should bring up your issue to a doctor to get better guidance on how to manage it. In terms of the science, I want to mention that in addition of being an excitatory (NMDA in the brain) and inhibitory (brainstem & spinal cord) neurotransmitter, glycine is also a very important amino acid so it is pretty much ubiquitous in the body. As such, it is hard to pin point why your supplement makes you feel awful.
@christinefarneman4433
2 ай бұрын
I saw another video on youtube about this and it might be because of to much chloride inside the cell instead of outside. When chloride rushes out of the cell after the binding of glycine it acts excitatory instead of calming.
@sciencewithtal
2 ай бұрын
@@christinefarneman4433 I guess this is a possible reason why but this is also something you cannot control (as far as I am aware). I still suggest you to get some medical advice!
@Pumiki
7 ай бұрын
12:03 The receptor is GABA-B and the subunits alpha-beta-gama combined are the Gi protein, right? So why does the receptor named "Gi"?
@sciencewithtal
7 ай бұрын
Good question, its just a matter of notation for me. I like to indicate on the receptor what G protein it recruits but obviously the receptor is not part of the G protein.
@learnwithme2315
10 ай бұрын
Is the chlorides equilibrium potential not around -60mV?
@sciencewithtal
10 ай бұрын
Yes, it can be. The equilibrium potential for chloride can vary quite a bit depending on its intracellular concentration. The value that is chosen in the video is 4 mM but in mammalian neurons it can vary between 4 and 30 mM.
@Nawwar.
8 ай бұрын
So with GIRK channels, they always lead to a pottasium efflux hence hyperpolarization? If so where does the name 'inward rectifier' comes from?
@sciencewithtal
7 ай бұрын
Hi, very good question! Sorry for the delay I had never seen your comment until now. Anyhow, here is my interpretation and to understand where I am coming from I suggest taking a look on Google at images of "inward rectifying iv curves": So, if you consider an IV curve with the voltage on the x-axis and the current on the y-axis, with positive values of y being an outward current (hyperpolarization) and negative values of y being an inward current (depolarization) you will notice that inward rectifiers produce an inward current only when the membrane potential is lower than the reversal potential of potassium (Ek) and when the membrane potential is above the channels produce an outward current. As you can see in the different pictures, the outward current that they produce is variable depending on the channel subtype. In my understanding, their use is sort of similar across the board. If we consider a neuron with a membrane potential (Vm) at -70 mV. When these channels open due to the mechanism explained in the video, they will lead to an outward current because Vm is greater than Ek. However, if the neuron gets hyperpolarized to lets say -85 mV and we assume for simplicity that Ek is -80 mV, then the channels will produce an inward current to buffer the hyperpolarization. So basically, these channels do produce both inward and outward currents but I think the name of inward rectifiers may have came because when you look at their IV curves, it is only the inward portion that is linear, which means that the channels can buffer the hyperpolarization at any membrane potentials but the same cannot be said about the outward current for most inward rectifier channels. I hope this makes sense and do not hesitate to correct me on anything!
@Blush-wu8zj
7 ай бұрын
Hello, I got a question about the inhibition of VGCC channels by GABA B! If I understood it correctly, this inhibits the transmitter release in the presynapse (snare complex needs calcium on synaptotagmin for exocytosis). What is meant by the presynapse, is it the presynapse of the next synapse, between the axoterminal of the cell whose dendrites have GABAb receptors and the next neuron? Or is it the presynapse of the same synapse, where GABA B was originally released? The latter doesnt seem to make sense because if GABA B is released less due to VGCC block, the postsynaptic cell would generate less IPSPs being rather excitatory? Thank you in advance!!
@sciencewithtal
7 ай бұрын
Hi, good question! It is the presynaptic terminal of the neuron that releases GABA. So basically this GABA B mechanism is autocrine (signals on the same cell). At 13:27 on panel 3 I show what it should look like. From my understanding, this mechanism is useful for the presynaptic cell to prevent releasing too much GABA and leading to over-inhibition.
@Blush-wu8zj
7 ай бұрын
@@sciencewithtal Thank you for your swift answer! 😊❤
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